title: Expression of c-kit in common benign and malignant breast lesions.
abstract: OBJECTIVE
  c-kit (CD117) is a transmembrane tyrosine kinase that acts as a type III receptor for mast cell growth factor. In recent years, the role of c-kit in the development of preinvasive and invasive breast carcinomas has been investigated. The aim of our study was to detect c-kit expression in the entire spectrum of common benign and malignant breast lesions in correlation with a well-studied myoepithelial or stem-cell like marker (p63).
  
  
  METHODS
  We evaluated 270 cases of benign and malignant breast lesions including fibrocystic disease, fibroadenoma, sclerosing adenosis, atypical ductal hyperplasia, ductal/lobular carcinoma in situ, and ductal/lobular/mixed type carcinoma. C-kit staining was evaluated in the cytoplasm/cell membrane in epithelial and myoepithelial cells and p63 in the nuclei of myoepithelial cells.
  
  
  RESULTS
  c-kit was highly expressed (85.3%) in benign lesions (fibrocystic disease, sclerosing adenosis, fibroadenoma), and p63 expression was 95.5% in the aforementioned lesions. c-kit distribution in preinvasive and invasive lesions was as follows: ductal/lobular carcinoma in-situ, 43%/35%; ductal/lobular carcinoma, 36%/39%; and mixed type carcinoma, 20%. c-kit was highly expressed in myofibroblast/fibroblast cells only in grade III ductal/lobular carcinomas. c-kit was totally absent in stromal cells in benign lesions and in situ carcinomas whereas expression was weak in grade I and II carcinomas.
  
  
  CONCLUSIONS
  Combined overexpression of c-kit and p63 is indicative of benign breast lesions. In contrast, there is reduced expression of c-kit in in situ and invasive breast carcinomas, with simultaneous overexpression in the stromal cells. This suggests that c-kit may play a role in breast cancer progression.
authors.affiliation: Department of Pathology, Aretaieion Hospital, University of Athens Medical School, Athens, Greece.
authors.forename: Agatha
authors.initials: A
authors.lastname: Kondi-Pafiti
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Arkadopoulos
authors.forename: Constantinos
authors.initials: C
authors.lastname: Gennatas
authors.forename: Vassiliki
authors.initials: V
authors.lastname: Michalaki
authors.forename: Matrona
authors.initials: M
authors.lastname: Frangou-Plegmenou
authors.forename: Paschalis
authors.initials: P
authors.lastname: Chatzipantelis
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000378:metabolism; D014408:Biomarkers, Tumor / Q000378:metabolism*; D001940:Breast / Q000378:metabolism / Q000473:pathology*; D001941:Breast Diseases / Q000378:metabolism* / Q000473:pathology*; D001943:Breast Neoplasms / Q000378:metabolism* / Q000473:pathology*; D018270:Carcinoma, Ductal, Breast / Q000378:metabolism / Q000473:pathology; D002285:Carcinoma, Intraductal, Noninfiltrating / Q000378:metabolism / Q000473:pathology; D018275:Carcinoma, Lobular / Q000378:metabolism / Q000473:pathology; D005260:Female; D018226:Fibroadenoma / Q000378:metabolism; D005347:Fibroblasts / Q000378:metabolism; D005348:Fibrocystic Breast Disease / Q000378:metabolism; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D006965:Hyperplasia / Q000378:metabolism; D007150:Immunohistochemistry; D008565:Membrane Proteins / Q000378:metabolism; D019009:Proto-Oncogene Proteins c-kit / Q000378:metabolism*; D012598:Sclerosis / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D015415:Biomarkers; D014408:Biomarkers, Tumor; C081876:CKAP4 protein, human; D008565:Membrane Proteins; D019009:Proto-Oncogene Proteins c-kit